Thu, 23 May 2019 14:38:11 -0700WeeblyFri, 05 Apr 2019 16:31:46 GMThttp://www.wellnessgarage.ca/blog/sleep-advice-for-seniors-or-anyone-for-that-matter(This post originally appeared in the Peace Arch News)I am a 78-year-old woman and my husband died last year. I’m getting used to living alone and have wonderful friends and a very supportive family. My only problem is that I’m having trouble sleeping at night. I can’t seem to fall asleep and then I wake up a number of times during the night. I don’t want to take sleeping pills but wondered if there is anything else I can do to improve my sleeping.

I’m glad that you’re doing so well adjusting to living alone and I think I can help you with your sleep. You are very wise to avoid sleeping pills as they frequently cause more problems than they solve.Your problem sleeping is shared by many; lack of sleep has become epidemic in our society and is increasingly common as we age. There are many causes for poor sleep, some of which need medical assessment, but mostly our ability to sleep well is within our control. Without knowing more about your physical and emotional health, here is a safe and proven framework for sleep. If you are not sleeping well after implementing this, a visit with your physician is warranted.

A good night’s sleep is all about optimizing your behaviours and environment to fit your body’s natural rhythm.

As humans we have evolved to be awake when it is light and to sleep when dark. Supporting this circadian rhythm are a cascade of different hormones that signal the body to be alert or sleepy. Our days start with a morning burst of the stress hormone cortisol, signalling that it is time to get up and greet the day. Over the course of the day our cortisol wanes, until in the evening our body releases melatonin to signal that it is time for sleep. Along with melatonin, levels of adenosine in the blood also tell us that we are tired. Adenosine is a by-product of energy expenditure – the more active we are the greater our levels of adenosine.

Your bed is only for sleeping (once you have re-established your sleep, you can try reading in bed again).

Finally, optimize your sleep ritual:

Two hours before bedtime, shut down the screens – TVs, computers and phones. The blue light from these devices will suppress your body’s release of melatonin and the content (especially the news) will often get your mind racing.

60 minutes before your bedtime begin a process to relax yourself – reading, light yoga, meditation followed by a sauna or hot bath. This ritual will help you wind down from the day, quiet your mind and set your body up for a great sleep.

Have fun with this – your sleep ritual should be a joy. Think of the rituals we create for our children – playtime after dinner, followed by a bath, a good read in bed and a loving tuck-in. We should all treat ourselves to such a nightly send-off.

Most often, adopting this framework is all it takes to restore sleep.

What do you do if this doesn’t work?This is where sleep restructuring comes in:

Go to bed at the same time every night.

Get up at the same time every morning

Since you are having trouble sleeping – do not nap.

Plan for a set amount of sleeping:

Calculate the total amount that you are currently sleeping (albeit broken) and use this to set your new sleep hours.

So if you are sleeping six hours in a broken fashion set your wake-up time exactly six hours after the time that you go to bed.

Then go to bed and wake up at the set times – no exceptions – even if you have had three hours of sleep you need to get up and start your day. You will be tired during the day but resist all urges to nap, come bedtime that fatigue will help you get to sleep.

Once you are sleeping soundly through that six hours, add 15 minutes to your sleep (go to bed 15 minutes earlier or set the alarm for 15 minutes later).

When you find that you are sleeping through the night and waking refreshed your sleep has been restructured. Generally, the total amount of sleep needed will be between seven and eight hours per night. Resist the urge to stay in bed longer than the sleep you need as this morning time slumber may result in your sleep deteriorating again.

At Wellness Garage we are here to support you in your health journey to take control of your health, restore confidence, and optimize your wellness. We do this through solid evidence-based medicine, personal health coaching and instruction, providing you with the knowledge, skills and support you need to apply healthy habits to your life.

]]>Mon, 11 Mar 2019 23:00:38 GMThttp://www.wellnessgarage.ca/blog/reconsidering-estrogen-replacement​For many physicians of my era (started practice in 1991) the story of hormone replacement therapy reflects the bandwagon nature of medicine. In the mid-nineties as I opened my practice, we actively recommended that almost all menopausal women should take hormone replacement (HRT) or estrogen replacement therapy (if they had a hysterectomy). As physicians we measured ourselves by our HRT percentage - feeling that if we were doing our jobs this should approach 100%.

...and while these benefits were offset by a small but real increased risk in venous blood clots - the benefits seemed overwhelming.

Then on July 17, 2002 the world of estrogen replacement came crashing down.

The Woman's Health Initiative - the largest and most expensive trial ($1B) ever done at that time was stopped because HRT increased the risk of breast cancer by 26%.

Overnight, physicians jumped off the bandwagon and rates of HRT fell dramatically.

Unfortunately most of us did not read the details of the study (once it was eventually released).

In the new book, "Estrogen Matters" by Dr. Avrum Bluming and Carol Tavris, the data from WHI is examined in the broader context.

Starting with the conclusion that HRT increases breast cancer by 26% - the first and most stunningly underappreciated fact was that this increase did not meet statistical significance, meaning that it did not clear the commonly accepted threshold that there has to be less than a 5% chance that this result could be random.

Next, even if you accepted that the result was real and not random, then it is important to understand the result. There are two ways that the study could have shown an increased rate of breast CA, either the rate of breast CA actually increased in the treatment group OR the rate of breast CA went down in the control group. Of course if the latter explanation is correct then the study is flawed.

Closer analysis of the WHI data has clearly shown that the reported increase rate of breast CA did not come from higher breast cancer rates than expected in the treatment group but resulted from the fact that the control group had a lower incidence of breast cancer than expected.

Even more confusing was the fact that this reduction of breast cancer in the control group occurred because there was a significant number of woman who had been on HRT previously and in this group there was less breast cancer.

So the WHI concluded that HRT increases breast CA because previous HRT experience decreased the rate of breast CA in the control group - incredible!

The third thing to consider when reviewing the WHI findings is the absolute rate of the increase in breast cancer.

So even if you accept that the effect is real and not the result of randomness or a decreased rate in the control group the absolute increase in was 8 more breast cancer diagnoses per 10,000 patient years.

Taken together, this review significantly decreases, if not removes altogether, the concern that I have about estrogen causing an increase in breast cancer.

Bluming and Tavris then revisit the benefits and risks of HRT - providing links to the best available current evidence and in doing so provide perhaps the best single source of HRT information for anyone considering HRT.

In the US that number is approximately 40,000, which is similar to the number of women who die in this country of breast cancer every year

Decrease in mortality from cardiovascular disease when started close to menopause - addition of 3-4 years of healthspan

Thisstudy by Nananda Colshowed that if every woman in the United States do hormone replacement therapy (HRT) it wouldincrease the median survival of women by 3.3 yearsin this country

Again it must be noted that there is a possible increased risk for women who begin HRT in their 60's with established atherosclerosis (at least in the first year) so HRT should be started at menopause.

When viewed from a numbers perspective the number of woman dying from heart disease is significantly greater than from breast cancer - so even if you accept that increased risk from the WHI study - the cardiovascular benefits will far outweigh that small absolute risk.

Decreased risk of dementia from 24% to 65% if started at the onset of menopause - data is mixed with starting after menopause and may result in worsening of dementia

"If neurons are healthy at the time of estrogen exposure, their response to estrogren is beneficial for both neurological function and survival. But if those neurons are not healthy when a woman starts estrogen or begins taking HRT ten or more years after menopause, estrogen may, over time make her condition worse" - Roberta Diaz Brinton.

Currently there is no treatment for Alzheimer’s

The one potential preventive medication is estrogen which can reduce the incidence of Alzheimer’s disease by between 20 and 50% depending upon the study you look at

The best osteoporosis strategy is to do everything to avoid the likelihood of falling, while providing the best lifestyle support to decrease the rate of bone loss.When it comes to osteoporosis, the strategy must be to decrease the consequences:

exercise to be stronger, more flexible and have better balance in order to avoid falling. The added benefit that exercise decreases the rate of bone loss helps but is not the main benefit.

maintaining adequate nutrition with appropriate calcium and protein is part of a healthy lifestyle - on its own it will have minimal effect on bone density and will not decrease the risk of fracture.

Vitamin D, like good nutrition, helps maintain bone health but will not on its own decrease fracture risk. It is part of a healthy lifestyle for many reasons beyond bone.

Calcium and Vitamin D are most important in teenagers and young adults, those who are in peak bone forming years.

Finally avoiding substance that increase the risk of falls (pain killers, alcohol, sleeping pills, and many prescription drugs) is essential.

It is important to remember that there are more fractures in people who do not have osteoporosis than in people that do; again reiterating the point that preventing the falls that cause the fractures is the most important thing you can do to decrease risk.

For woman at risk for osteoporosis, there is an additional strategy that must be considered - estrogen.

For maintaining bone mass there is no other therapy as effective as estrogen replacement starting early in menopause.

For both women and men - peak bone mass is achieved in early adulthood, and through an active lifestyle, with adequate nutrition (calcium and protein), and Vitamin D, maintained until middle age when it begins to drop more rapidly.

For women, the dramatic fall in estrogen levels (to 1% of pre-menopausal levels) is largelyresponsible for most of the bone loss, and replacement therapy is very effective at decreasing this rate of bone mass.

More importantly, estrogen replacement therapy has been definitively shown to decrease fractures.

Estrogen replacement can reduce fractures from 33-50%.

Most importantly this reduction also applies to hip fractures - recall that approximately 28% of women will die within 1 year of fracturing their hip.

Estrogen replacement combined with exercise (which can also reduce risk of hip fracture by 38%) makes sense for any woman at high risk of osteoporosis.

Of course a recommendation of estrogen replacement comes with some important considerations:

there is a need to take estrogen for at least 10 years and likely forever

estrogen has other risks and benefits that need to be considered on an individual basis

In our next post, we will review the broader topic of hormone replacement, exploring the risks and benefits.

At Wellness Garage we are here to support you in your health journey to take control of your health, restore confidence, and optimize your wellness. We do this through solid evidence-based medicine, personal health coaching and instruction, providing you with the knowledge, skills and support you need to apply healthy habits to your life.

One in three women and one in two men will suffer an osteoporotic fracture in their lifetime.

80% of all fractures in people over the age of 50 are aconsequence of osteoporosis.

Of the various osteoporotic fractures, hip fractures are the most devastating:

30,000 Canadians fracture their hips annually, with 70-90% due to osteoporosis.

Of these, 28% of women and 37% of men will die within one year of breaking their hip.

Unfortunately, all too often, a fracture is the first indication that a person is affected by osteoporosis.

To understand why osteoporosis happens and to develop a strategy to prevent its consequences, we must understand how bone works.

Last week we reviewed the dual, competing functions of bone:

Bone acts as structure as well as reservoir for calcium and phosphorus act in competition. Bones must be strong and flexible to respond to the weight bearing and mechanical forces of our activities. When our activities increase in intensity, our bones get stronger in order to sustain the load. However if calcium or phosphorus are in short supply, our regulatory hormones will draw them out of bone to serve vital function in other cells in the body, and in the process potentially weaken bone.

Bone is an incredible material providing both strength and flexibility in order to be resilient to the mechanical forces imposed by daily activities. To accomplish this bone is a composite material made of minerals bound to protein, predominantly collagen. If bone was made only from mineral crystals it would be brittle and fracture easily; if made solely from protein it would be too flexible and would not provide adequate structure and flexibility.

Bone is also a dynamic material always changing and growing, responding to mechanical loads, resorbing and laying down new bone through the balanced effects of osteoclasts and osteoblasts.

During our childhood, as our bones are growing both cell types are constantly working, osteoclasts reshaping and osteoblasts rebuilding bone with osteoblast activity predominanting so that bone length, thickness and overall mass increase as our bodies grow in stature.

Once growth is finished and we are adults, osteoblasts spend less time creating new bone and more time regulating bone repair - osteoblasts signal osteoclasts to hollow out bone in a specific location and then fill in that area with new & healthy bone.

To build and maintain our bones three general principles emerge:​

Use your bones to increase their strength

"use it or lose it" applies to your bones

Supply your body with the key ingredients to develop bone

Osteoblasts use calcium to build new bone, calcium comes from the food we eat and requires adequate Vitamin D for absorption. (for more on Vitamin D - see these previous blog posts:

Bone formation is also dependent on adequate protein intake to build the collagen-hydroxyapatite bone matrix.

Finally Vitamin K2 is necessary to for activating proteins released by the osteoblasts that draws calcium into the bone matrix. (Vitamin K2 is generally produced by bacteria in our GI tract - so another reason to maintain gut health.)

Avoid substances that decrease bone strength:

tobacco - smokers lose bone density sooner than non-smokers

alcohol - 3 or more drinks per day can increase bone loss

colas - the phosphoric acid in colas leaches calcium from bones. (our partner BodyComp have numerous case studies of young people with decreased bone density due to excessive cola consumption).

some medications

excess thyroid replacement

corticosteroids

Osteoporosis has been described as a pediatric disease with geriatric consequences, because our bone mass peaks when we are young (16-20 in women, and 20-25 in men).

As young adults, our goal is to maintain bone density and strength through the three principles.

But even with excellent bone habits, we all begin to lose bone in our mid 30's.

For woman the situation is more challenging as the precipitous drop in estrogen that occurs in menopause causes rapid bone loss, and is the reason why woman are more affected by osteoporosis than men.

So, the question for middle age to older people is how do the three principles work to avoid the consequences of osteoporosis?

The key here is to think about more than bone density, to develop a strategy to decrease the consequences of osteoporosis: debilitating and life shortening fractures.Looked at from this angle - Principle 1 - use your bones to increase their strength is most important.

Moderate to vigorous exercise is associated with a 45% and 38% reduction in hip fractures in men and women respectively. Exercise helps slow the loss of bone that comes with ageing in both men and women, but this is not how it decreases hip fracture risk. Exercise works by reducing the risk of falling in the first place.

Developing an exercise strategy that focuses on maintaining strength, functional movement and balance is the best thing you can do to avoid the consequences of osteoporosis - regardless of bone density.

What about Principle #2 - supplying your body with the key ingredients to develop bone?

This is absolutely key in the bone developing years as teenagers and young adults, and likely important through middle age, but it is not sufficient to decrease fracture risk. A systematic review published in 2015 by Boland et. al concluded that "dietary calcium intake is not associated with risk of fracture, and there is no clinical trial evidence that increasing calcium intake from dietary sources prevents fractures. Evidence that calcium supplements prevent fractures is weak and inconsistent."

Complicating matters further, there is some evidence that calcium supplements may be associated with cardiovascular risk though the evidence is inconsistent and inconclusive. Many clinicians have moved away from recommending calcium supplements, instead recommending that adequate calcium intake be achieved through nutrition. Given the high calcium content of green leafy veggies - this is definitely the position we take.

As for Vitamin D, there are so many benefits of "D" beyond bone that the lack of clinical trial evidence to support a reduction in fracture reduction, does not change our view that maintaining optimal Vitamin D levels must be part of any strategy for long term health and vibrancy.

Finally avoiding substance that increase the risk of falls (pain killers, alcohol, sleeping pills, and many prescription drugs) is essential.

Decreasing bone density is an inevitable part of ageing - our bone density peaks in our early years, is maintained up to middle age and declines thereafter. If we live long enough, our bones will become thinner. Whether they reach the diagnostic levels of osteoporosis is less important than our ability to avoid falling.

The best osteoporosis strategy is to do everything to avoid the likelihood of falling, while providing the best lifestyle support to decrease the rate of bone loss.

While this advice applies equally to men and women, we have left out something for women - the role of estrogen in bone loss and osteoporosis, and the risks and benefits of estrogen replacement as an osteoporosis strategy...more on this next week.

At Wellness Garage we are here to support you in your health journey to take control of your health, restore confidence, and optimize your wellness. We do this through solid evidence-based medicine, personal health coaching and instruction, providing you with the knowledge, skills and support you need to apply healthy habits to your life.

]]>Fri, 18 Jan 2019 22:51:01 GMThttp://www.wellnessgarage.ca/blog/the-science-of-bone-health-3-principles-to-develop-maintain-boneIn preparation for our Bone Health event on Feb 27th - this is the first in a 3 part series on Bone Health.

Our bones are remarkable examples of evolution's ingenuity. From a functional perspective, bones serve multiple roles - structure, mobility, support, protection as well as serving as a reservoir for essential minerals. These roles became important, when our distant predecessors left the calcium-rich ocean to live in calcium-poor fresh water, and then further evolved to live on land where gravitational forces (without the buoyancy effect of water) put greater stress on the skeleton.

Our skeletons store two key minerals, calcium and phosphorus, both essential for the healthy functioning of cells and bodily organs, and our bones are called, in times of stress, to maintain blood levels of both. A complex system of hormones regulates calcium and phosphorus in our bodies acting on bone, intestine and kidneys to maintain adequate supply for proper cellular function in all cells but particularly in nerves and muscle.

Vitamin D - acts on the intestines to absorb calcium and on the osteoclasts to resorb bone and maintain blood calcium levels thereby keeping PTH in check.

Calcitonin - released by the thyroid, calcitonin decreases osteoclast activity and decreases resorption of Calcium and phosphate from the kidneys

Sex Hormones

Estrogen - In both males and females, estrogens play a key role in bone maturation and maintenance of bone density. The drop in estrogen in menopause leads to dramatic bone loss in women. (more on this to come)

Growth Hormone & Insulin-Like Growth Factor (IGF-1) - most of the effect of growth hormone is through the GH dependant secretion of IGF-1 from the liver. IGF-1 acts on osteoblasts to increase bone formation.

This dual roles of bone, to act as structure and at the same time represent a reservoir for calcium and phosphorus, are in direct conflict with each other. Bones must be strong and flexible to respond to the weight bearing and mechanical forces of our activities. When our activities increase in intensity, our bones get stronger in order to sustain the load. However if calcium or phosphorus are in short supply, our regulatory hormones will draw them out of bone to serve vital functions in other cells in the body, and in the process potentially weaken bone.

Bone is an incredible material providing both strength and flexibility in order to be resilient to the mechanical forces imposed by daily activities, not to mention sports. To accomplish this bone is a composite material made of minerals bound to protein, predominantly collagen. If bone was made only from mineral crystals it would be brittle and fracture easily; if made solely from protein it would be too flexible and would not provide adequate structure and flexibility. The mineral components of bone are crystals of calcium and phosphate called hydroxyapatite. They are bound in a matrix to a triplet of three long, thin, intertwined collagen rods with are strengthened by chemical bonds between proteins. Other proteins further strengthen the collagen matrix and regulate mineral binding. Small changes in shape of the bones, from mechanical forces, act on the cells inside the bone to send signals that allow bone to respond to these loads by remodeling and strengthening.

In this way, our bones are always changing and growing, responding to mechanical loads, resorbing and laying down new bone.

Bone health depends on the balanced effects of two kinds of bone cells:

Osteoblasts - the cells that make bone and

Osteoclasts - the cells that dissolve and remove old bone

During our childhood, as our bones are growing both cell types are constantly working, osteoclasts reshaping and osteoblasts rebuilding bone with osteoblast activity predominating so that bone length, thickness and overall mass increase as our bodies grow in stature.

Once growth is finished and we are adults, osteoblasts spend less time creating new bone and more time regulating bone repair - osteoblasts signal osteoclast to hollow out bone in a specific location and then fill in that area with new & healthy bone.

Bone also has another remarkable feature - it is anti-fragile: if stressed it gets stronger. This phenomena, called Wolff's Law was originally recognized in late 19th century, but is probably most dramatically visualized in tennis players who show far greater bone mass in their racket arm as compared to their non-dominant arm.

This remarkable gift, that our bones grow stronger through stress and usage has a dark, flip side: our bones grow weaker through disuse.

Only in modern times has this become a downside. For most of human history, our lives were simply too active. Our predecessors had very strong bones from all the physical work and stress placed on their bones throughout their lives. From the industrial revolution on onward, labor saving technologies have decreased the degree to which we need to use our bodies to the point that many of us are no longer building enough bone. This is another example of evolutionary mismatch that I have previously written about.

Compounding this fundamental mismatch, modern diets and lifestyles also lead to deficiencies in dietary calcium, protein and Vitamin D necessary for bone health.

Bone formation is also dependent on adequate protein intake to build the collagen-hydroxyapatite bone matrix.

Finally Vitamin K2 is necessary to for activating proteins released by the osteoblasts that draws calcium into the bone matrix. (Vitamin K2 is generally produced by bacteria in our GI tract - so another reason to maintain gut health.)

Avoid substances that decrease bone strength:

tobacco - smokers lose bone density sooner than non-smokers

alcohol - 3 or more drinks per day can increase bone loss

colas - the phosphoric acid in colas leaches calcium from bones. (our partner BodyComp have numerous case studies of young people with decreased bone density due to excessive cola consumption).

some medications

excess thyroid replacement

corticosteroids

Next week, we will look at osteoporosis and what you can do to prevent or reverse it.

At Wellness Garage we are here to support you in your health journey to take control of your health, restore confidence, and optimize your wellness. We do this through solid evidence-based medicine, personal health coaching and instruction, providing you with the knowledge, skills and support you need to apply healthy habits to your life.​If you feel that you need help, please book a free consultation with us to learn more.

]]>Thu, 10 Jan 2019 21:49:31 GMThttp://www.wellnessgarage.ca/blog/the-strange-evolutionary-tale-of-uric-acid-why-a-genetic-adaptation-16m-years-ago-may-be-leading-to-21st-century-obesity16M years ago, our common ancestors were European apes living in subtropical Europe. A major global climate change occurred, cooling and altering the environment in which they lived.

Evolution in its brilliant but blind way, adjusted and left man to evolve with a genetic change that is now haunting us.

The change was a progressive sequence of loss of function mutations that rendered an enzyme called uricase inactive and allowed uric acid levels to soar in these apes, and everything that followed in their evolutionary line.

Uric acid, in so much as you have ever heard or thought of it, is likely linked in your mind as the compound that in excess triggers gout.

When we think of gout, images of Henry VIII eating a drumstick, gorging himself with meat and alcohol come to mind. Acute gout, the process where uric acid crystallizes within the joints, strangely enough most commonly at the base of the big toe, was until the 20th century largely the disease of kings. Only the very wealthy could afford the lifestyle of excess that allowed uric acid levels to soar and subsequently crystallize.

In the latter half of the 20th century, the incidence of gout, and other uric acid related diseases, has begun to soar as Western diets - high in purine proteins (meat & seafood) and beer has become more common. The real culprit though is likely the increase of dietary fructose from added sugars. But I'm getting ahead of myself...

What is unusual about gout is that it is a human disease - in fact, most mammals have very low levels of uric acid because they have the enzyme uricase that converts uric acid into a more water soluble form that is easily excreted by the kidneys.

In addition to gout, elevated uric acid is also associated with hypertension, endothelial dysfunction, metabolic syndrome, kidney and liver disease.

So why would evolution have humans lose such a key enzyme?

Evolutionary scientists have some ideas, as they have traced the uricase mutation to European apes living in subtropical Europe 16M years ago.

At that time, these apes, who were our ancestors, thrived in subtropical Europe on a diet predominantly consisting of fruit. A global cooling event at that time caused a rapid decrease in the availability of fruit in Europe and was the likely trigger for the mutation.

This is where it gets really interesting - one of the metabolites of fructose is uric acid, increases in uric acid cause a shift in mitochondrial metabolism, and result in increased fat storage. At times of stress, where fructose consumption was going down, increasing fat storage would be a desirable effect, increasing the likelihood of survival. Higher uric acid levels contribute to greater fat storage.

At the same time, with decreases in fruit availability, Vitamin C consumption would have decreased for these apes. Vitamin C is a powerful anti-oxidant and one that apes would rely on.

One paradox of metabolism is that we need oxygen to generate energy from food but oxygen is highly reactive and through the creation of reactive oxygen species (ROS) damages cells and DNA - this toxicity related to oxygen is called oxidative stress and is associated with over 100 different diseases. To protect against oxidative stress - we have through evolution developed many protective strategies - including Vitamin E, beta carotene, glutathione, Vitamin C and .... uric acid.

Interestingly, uric acid is a powerful anti-oxidant and provides almost 50% of our circulating anti-oxidant capability. So as Vitamin C levels went down, due to decreased fruit consumption, secondary to global cooling, from a survival basis a mutation that increased uric acid levels to essentially replace the antioxidant capacity lost from decreased Vitamin C levels makes sense. Ironically, our ability to synthesize Vitamin C was previously lost in evolution - perhaps in response to plentiful dietary "C" from fruits!

A third survival benefit to the loss of uricase relates to uric acid's ability to maintain blood pressure in a low salt environment, which may have also been a by-product of the climate changes 16M years ago. This blood pressure effect may also have been instrumental in enabling humans to walk on two legs with their heads significantly above their hearts.

Evolution selects for mutations that increase survival in the presence of threatening environmental challenges (this is natural selection):

elevated uric acid can help compensate for decreased caloric intake from decreased fruit intake through its physiological ability to favour increased fat storage - essentially a thrifty gene for times of food shortage

elevated uric acid can compensate for a loss of antioxidant capacity due to decreased Vitamin C production

elevated uric acid can maintain blood pressure in an environment where salt intake has decreased.

But what happens when modern living dramatically changes the food environment?

rapid shifts from a low caloric environment to a high caloric environment

specific dietary increases in fructose - in the form of added sugars (remember table sugar - sucrose is made up of fructose and glucose) and high fructose corn syrup - a key ingredient in many processed food choices.

What happens is that our genes work against us, and in our current food environment, uric acid levels are soaring resulting in soaring rates of chronic diseases:

obesity

metabolic syndrome

hypertension

endothelial dysfunction

heart disease

in addition to gout...

Our genes through natural selection are matched to our environment - the tragedy of modern life is that in less than 100 years, we have created evolutionary mismatches across all key human behaviors: nutrition, exercise, sleep, stress tolerance, relationships and purpose.

The bad news is that these mismatches are responsible for much of the epidemic of chronic disease that we face.

The good news is that we, as individuals, have the ability to make choices that better match our genes.

In the case of uric acid, eliminating fructose from added sugars and high fructose corn syrup and consuming alcohol in moderation are the places to start. Maintaining healthy proportion of protein (around 20% of calories), hydrating as well as consuming enough Vitamin C from foods.

Bottom Line:Synopsis:Evolution has led humans to have high levels of uric acid (relative to other mammals). The benefits of the evolutionary change are challenged by the hyper caloric, high fructose world we live in now - resulting in high levels of obesity and soaring uric acid triggering metabolic syndrome, hypertension, endothelial dysfunction, and worsening Type II Diabetes.

What to Do:

Know your uric acid level:

Optimal < 250 umol/L

Increased Risk 250 - 300 umol/L

High 300 - 430 umol/L

Very high > 430 umol/L

Make changes to your nutrition:

decrease/eliminate added sugars from your diet

reduce/eliminate refined carbs

moderate alcohol consumption

increase hydration

get adequate Vitamin C - from fruits and veggies

​Take Control of Your Health:

At Wellness Garage we are here to support you in your health journey to take control of your health, restore confidence, and optimize your wellness. We do this through solid evidence-based medicine, personal health coaching and instruction, providing you with the knowledge, skills and support you need to apply healthy habits to your life.

]]>Mon, 31 Dec 2018 08:00:00 GMThttp://www.wellnessgarage.ca/blog/end-of-2018-reflectionsAs the year closes, and the Garage is closed until the New Year, it is a great time to reflect on 2018.It's been eight months since the Garage opened, and already we have witnessed so many health transformations.​Our members are a diverse lot - ranging from 23 to 79 years of age, almost evenly split between men and women. Many have sought our help to restore their health - reversing their diabetes, controlling their blood pressure and decreasing elevated cardiac risk. Others have come to us to regain confidence in their health, lose weight and get in better shape. While some leverage our precision lifestyle medicine tools to optimize their health, fitness and performance

.A few stories stand out...(these members have consented to share their stories - names and initials have been changed to protect privacy)

FJ - a 57 year old man with Type II Diabetes came to us looking for help with using a ketogenic diet to address his diabetes. He had read about the amazing reversals and remissions achieved through a low carb, high fat nutrition strategy. As a retired paramedic and first responder, he also realized that diabetics on high doses of insulin should approach intensive therapeutic nutrition with medical supervision. During our assessment, one of the first things that we did was check his C Peptide levels to ascertain was whether his pancreas was still producing insulin. His levels were low, indicating advanced diabetes with pancreatic fatigue, but they were high enough to encourage us that reversal was still possible. After completing our Comprehensive Lifestyle Medicine Assessment, our approach was actually simpler than recommending the ketogenic diet that FJ had originally sought from us. Instead when we reviewed his behaviors, we decided to take a more graduated approach to his nutrition. As I explained, we should start with the elimination of added sugars, refined carbohydrates, bread, pasta and white rice; add an element of time restricted eating (at least 12 hours without calorie consumption) and moderately increase exercise towards 150 minutes per week, and wherever possible increase activity. Even though these changes were not as aggressive as an immediate adoption of the keto diet, I still recommended that FJ reduce his insulin by 40% to avoid low blood sugars.

The changes were immediate - blood sugars that had been reading in the 15+ mmol/L range dropped down to 5-7 mmol/L. The first few weeks transitioning to this way of eating were tough for FJ but he as he commented: "the support from the Wellness Garage team made this easier". After a few weeks, the cravings that had thwarted other previous attempts to change his eating went away. The changes no longer seemed hard, they were now the new normal.

When FJ started his major symptom was chronic pain - "Old injuries in my elbow, lower back, and hip regions would wake me up at nights and bother me throughout the day." After weeks with his new nutritional habits, his pain disappeared. His diabetes, which had been diagnosed over 25 years ago, and had progressed to the place where he was taking over 200 units of insulin per day with a continuous insulin pump, had dramatically improved.

In 4 months his HbA1C has improved from 11.9% to 6.5%, while his insulin dose dropped to 60 units per day, his cholesterol has improved by 19%; triglycerides by 81% and his TG/HDL - a measure of insulin sensitivity (and likely a predictor of ongoing improvements) has improved by a stunning 85%. Even more encouraging, his C-peptide levels returned to normal, indicating recovery of pancreatic beta islet functionality.

...and he has lost 25 lbs (3 pant sizes smaller!)

All this without calorie counting or strict restrictions - just real food, not too much, coupled with increased activity.

In the next few months, FJ plans to work on increasing his exercise gradually, which should be easier now that his chronic pain has resolved and he has lost some weight.

Almost as dramatic is the story of JW, a 26 year old woman who was referred by her neuro-opthalmologist. JW, a former athlete, had gained over 100 lbs in the past 3 years and was suffering from intense migraine headaches multiple times a week. At her initial consultation, she weighed over 350 lbs and said she felt trapped because of lack of resources. She and her husband were living on a $200/month grocery budget and as a result were eating a lot of refined carbohydrates (especially pasta) as well as fast food. Her initial workup, revealed that JW was now diabetic with mildly elevated blood sugars and HbA1c. With this diagnosis and her circumstances, what she really needed was nutritional coaching at a very practical level to help her eat real, whole food on her $200/month budget. With a bit of ingenuity along with some trial and error, JW learned to make different choices at the grocery store and different meals at home. Her ability to focus, and her drive to get healthy allowed her to make the changes within weeks. Again, her results have been dramatic - 50 lbs weight loss in 6 months, coupled with a reversal of her Type II Diabetes. Her headaches are almost all gone, and she is getting ready to return to work.

ST, a 32 year old police officer with a traumatic brain injury came to the Garage as part of a weight management program. He was suffering from regular headaches, fatigued and irritable. For ST, the nutritional approach was pretty simple - increase his veggies, decrease his refined carbohydrates, help him plan for healthy snacks all while gradually increasing his running (paired with some strength and yoga work). In 4 months he lost 23 lbs, the headaches, fatigue and irritability were greatly improved, and the running was going so well that ST shifted from restoring his health towards optimization by setting a goal of a 2019 marathon. In reflecting on these changes, ST said:"After the injury I felt like so many things had been taken away from me. Focusing on my health has given me a sense of control back in my life."

The final quick story, I will relate is that of HL a 62 year old marathoner who came to the Garage to see if there was anything he could learn to improve his running performance. His DXA showed a bit more abdominal fat than was expected and the nutritional assessment found a few simple changes that could help. Within months, WL found he had dropped back to his university weight and his running times were his best in 8 years. Simple changes - big results.

In the eight months since the Garage opened we have been privileged to help many on their healthy journeys and the transformational changes that we are seeing are really quite stunning. The improvements in weight, blood pressure, cholesterol, blood sugars and cardiac risk are at levels well beyond what any drug or drug combination could ever realize. What we are witness to is the body's profound resilience and ability to return to health when simple behaviors are changed.

Nothing that we recommend at Wellness Garage is radical - instead it is the application, and stacking of many small habits, that one by one help restore the body's natural homeostasis and optimal health.

All of these amazing results have come from people, taking control of their health, one habit at a time.

The hard work is done by our members, we are their pit crew to support them on their health journey.

As 2018 closes, and I look back at the year, I am very grateful to have participated in so many transformations and look forward to more to come.

If you, or someone you know, is looking to make 2019 the year that you restore or regain confidence in your health - please reach out or tell others about Wellness Garage. We welcome everyone with a free initial consultation where we can discuss how we can help.

]]>Mon, 26 Nov 2018 20:24:33 GMThttp://www.wellnessgarage.ca/blog/low-carb-diets-is-there-a-metabolic-advantage​Two weeks ago, another major shot was fired in the war between those who believe that decreasing carbohydrates are essential to weight loss, and those who believe low carb is no better than any other method of weight loss.

The study, by all accounts, was impressively executed (at the cost of $12M), and was designed to determine whether low carbohydrate diets had any advantage in terms of total energy expenditure as compared with medium and high carbohydrate diets. Simply said - is there a metabolic advantage, where your basal metabolism burns more energy per total calories consumed on one diet vs the other.

Advocates of the low carb approach to weight loss and weight maintenance subscribe to a physiological theory known as the carbohydrate-insulin model of obesity, where increased the increased ratio of insulin to glucagon after high glycemic meals directs fuels into storage in adipose tissue. The rapid storage of fuels as fat leads to increased hunger and food cravings, and decreased energy expenditures, predisposing to weight gain. In this model the degree of weight gain should correspond to the insulin level - as higher insulin levels lead to greater fuel storage. The theory provides an explanation for the global obesity trend as people have increased their consumption of high glycemic refined carbohydrates over the past 30 years.

The theory has some eloquent supporters, most notably journalist Gary Taubes, who founded the Nutritional Science Initiative (NuSi) to do the science necessary to prove or disprove the theory.

Until now, existing data has not provided support for this theory, with perhaps the greatest challenge coming from a NuSi study led by Kevin Hall, which was done under the controlled settings of a metabolic chamber.

Despite the lack of evidence from controlled feeding studies, supporters of the carbohydrate:insulin theory have maintained that studies were not long enough - most were only two weeks, and the process of adaptation to a low carb diet takes at least 2-3 weeks - or they were technically flawed (or both).

On the other side of the debate, many researchers and nutritionists point to the many real-world studies that have failed to show that low carb has any benefit over any other approach (ie. Mediterranean diet, Zone, low fat, etc.).

Since the study was about weight maintenance, all subjects (164 adults aged 18-65 years with a BMI >25) were put on the same weight loss diet with the goal of 12% weight loss (within 2%). After the run-in weight loss, the subjects were randomized to to three test diets according to carbohydrate content (high, 60%; moderate, 40% or low 20%). Each test diet was controlled to deliver the same amount of protein (20%) and were adjusted to maintain weight loss.

The results were supportive of the carbohydrate-insulin model:

those subjects on the low carb diet burned an extra 278 kcal/day compared to those on the high carb diet

if the subject had higher levels of insulin, a measure of insulin resistance, the effect was more dramatic - those on the low carb diet burned an extra 478 kcal/day

While these results seem to confirm the carbohydrate:insulin hypothesis, other researchers are not yet ready to concede. Kevin Hall, the researcher that led the original metabolic chamber, NuSi trial that failed to demonstrate any metabolic advantage to a low carb diet, and a known skeptic of the carbohydrate:insulin theory, has pointed out a potential methodological issue with the trials. He points out that the method that the researchers used to measure energy expenditure is less reliable when weight is changing - so the proper comparison for diet effect should be the difference between energy expenditure at the beginning of the trial, before any weight loss, compared to the weight at the end of the trial. Instead, the study compared the effects after the weight loss, and before randomization into the three experimental groups. If you look at the data from Hall's viewpoint, the metabolic advantage shrinks to less than 100 calories - an effect that may not be statistically significant.

Others point out that in the real world low carb diets do not outperform other diets when it comes to weight maintenance, and that this trial screened over

Still these findings are intriguing as they provide some evidence for the claim made by low carb proponents that low carb is easier than any other diet.

Healthline has an excellent review of 23 randomized controlled studies that shows an edge towards low carb, but many studies are very hard to assess because of variability in nutrient quality - DIETFITS was perhaps the best designed study to compare healthy low fat with healthy low carb - it essentially found no difference between groups.

with low carb diets - the focus is no restricting carbohydrate intake - with low fat the focus is to restrict total caloric intake and fat intake. Both approaches have similar compliance rates.

Observational studies show a potential increase in all-cause mortality with low carb diets but controlled trials show no adverse effects up to 2 years and no adverse effects from a biomarker perspective with the exception of increased LDL-C, which is offset by an decrease in LDL-P.

As with any diet - most of the benefit is in stopping the consumption of added sugars, refined carbohydrates and junk food,

Solely focusing on macronutrients can be potentially harmful if it ignores food quality - neither pepperoni nor pepsi are healthy even though one could say they fit into a LCHF and a LFHC diet respectively.

While there are debates about LCHF and LFHC - there should be no debate that a HFHC is the real issue in our society today. Too many people are eating too many calories from poor quality sources high in both fat and carbohydrates. This simply put is the cause of obesity in our society.

Try as we might to learn more about nutrition, nothing beats the the simple rules laid out by Michael Pollan, in his book "In Defense of Food":

Eat Real Food

Not too much

Mostly plants

#takecontrolofyourhealth

At Wellness Garage - we can help you understand, and take control of your health. Our comprehensive medical, fitness, nutritional and behavioral assessments give you baseline from which to measure your progress. Our coaching helps you improve your behaviors, one habit at a time.

]]>Fri, 16 Nov 2018 17:22:41 GMThttp://www.wellnessgarage.ca/blog/a-better-way-to-get-vitamin-d-in-the-winterWith the end of daylight savings, once again we are reminded that we are beginning the dark days of winter when we no longer can rely on the sun to get our Vitamin D.

Vitamin D is essential for human health. Best known for its role in calcium metabolism and bone health, Vitamin D deficiency has been implicated in over 100 different disorders ranging from heart disease, hypertension, both Type I and Type II diabetes, depression, cancer, auto-immune disease, and multiple sclerosis. Vitamin D receptors are found in almost every type of human tissue.

During the summer, we are able to synthesize Vitamin D through the stimulus of mid-day sunlight on our skin. Specifically, the UVB rays in sunlight catalyze the conversion of 7-dehydrocholesterol into cholecalciferol - Vitamin D3. Vitamin D3 travels through the blood, via Vitamin D binding protein to the liver where it is converted to 25(OH) D which then circulates to the kidney and other tissues to be converted into the active form of Vitamin: 1,25(OH) D.

At our northern latitude, UVB strength is not sufficient from October to March for us to generate Vitamin D, so we need to get our "D" from our diet. Unfortunately, very few foods contain significant amounts of vitamin D (fish, shiitake mushrooms being exceptions). To address this, most dairy products have been fortified with Vitamin D. Despite this, most Canadians get insufficient Vitamin D levels for optimal health.

At Wellness Garage - we recommend that everyone supplement with Vitamin D from October to March. Until recently, our recommendation was to take 2000 IU of high quality Vitamin D daily.

We now have a better way for our members to get their Vitamin D: the Solius light booth.

Solius was designed to deliver the specific frequency of UVB light that stimulates Vitamin D production in the skin without the risk of sunburn. By targeting and isolating specific UVB frequencies, only 0.15% of the sun's spectrum, Solius maximizes the efficacy of Vitamin D synthesis with extremely low ultraviolet exposure. Put in perspective, one 3 to 4 minute Solius treatment, on average, provides the same amount of UV radiation as 9 seconds of midday summer sunlight, yet synthesizes enough Vitamin D for a week!

The greatest risk from UV radiation comes from UVA exposure - in fact tanning beds deliver greater than 95% UVA and greatly increase the risks of developing skin cancers. UVB light sources minimize UVA and have not been associated with increased cancer risk. Compared to other UVB sources, Solius further reduces exposure to overall UV radiation through its patented delivery system.

Solius is the safest way to produce Vitamin D naturally.

One Solius treatment weekly is all that is needed to optimize your Vitamin D. There is no risk of over or under treatment with Solius, since light is the natural input for Vitamin D production. Just as there is no danger of excess Vitamin D from a day in the sun, Solius, by leveraging the body's natural feedback mechanisms avoids the risk of super physiological doses. Vitamin D3 produced in the skin delivers a slow and steady dose of pro-hormone to the liver that is distinctly different from the absorption of supplements from the intestine.

While Solius prevents "over-dosing" of Vitamin D, under-dosing is the more prevalent issue for most people supplementing. At the recommended daily dose of 600 IU (800 IU for age > 70) many people do not reach adequate Vitamin D levels. Since Solius triggers the body's natural response and feedback system - optimal physiologic levels are achieved.(for more on the variation of Vitamin D levels - see our previous post on Vitamin D).

Wellness Garage is fortunate to have one of only two Solius booth's deployed (there will be many more to come). To experience Solius - download the Solius app from the Apple or Google Stores), register and book through the app.

For those of you that do not have a Solius near by and still need to supplement, here are our recommendations:

At Wellness Garage - we can help you understand and take control of your health. Our comprehensive medical, fitness, nutritional and behavioral assessments give you baseline from which to measure your progress. Our coaching helps you improve your behaviors, one habit at a time.

The etiology of atherosclerosis, the disease process underlying heart disease and stroke - the #1 cause of death and disability in Canada.

There were a number of takeaways that are worth reiterating:

Atherosclerosis is a process that takes place over decades - and can be thought of as systemic, potentially affecting all arteries, starting in childhood.

Thinking of heart disease as a “clogged pipe” problem is misguided as most atherosclerotic lesions that cause harm - heart attacks and death - are in arteries with minimal or moderate narrowing.

Focusing only on arteries that are narrowed - through surgery and stents - can miss the point that atherosclerosis is a systemic process that needs to be dealt with systemically.​

​Atherosclerosis involves a reinforcing cycle of:

Endothelial dysfunction leading to the

Oxidation and retention of lipoproteins in the subendothelial space leading to

Inflammation resulting in further

Endothelial dysfunction​

This deeper understanding of the disease helps us understand why most cardiac events happen in people with normal LDL cholesterol. LDL particles (LDL-p) are necessary but not sufficient to cause disease.

Higher LDL-p levels correlate with higher risk - because more LDL-p can get into the subendothelial space (ie. under the arterial lining), where they can get stuck, oxidized and trigger the inflammatory process that underlies atherosclerosis.

In a person with normal endothelial function, LDL-p go into, and out of the endothelial space all the time, without resulting atherosclerosis. Some degree of endothelial dysfunction is therefore necessary for the trapping and oxidation of LDL-p and the resulting inflammatory cascade.

Finally, it is the inflammatory response that causes all the damage. Increased levels of systemic, chronic inflammation, amplify this effect. Similarly, low levels of circulating inflammatory molecules and cells, decrease the proliferation of atherosclerotic lesions.

This week we will get very practical and provide a framework for understanding risk and treating, preventing or reversing atherosclerosis.

The first objective is to understand your risk. Since atherosclerosis is a process involving:

Endothelial dysfunction

Oxidized LDL

Inflammation

A perfect risk model would take all three into consideration.The challenge is that we do not have perfect metrics, with enough evidence in relation to the hard outcomes of cardiac events to be definitive.

Here we can rely on some evidence-based risk calculators, like Framingham, that are based on large datasets. These generally are a good place to start:

Framingham - takes into account

Age - since the risk of atherosclerosis is a probabilistic time dependant function - age is the single biggest risk factor. Expose endothelial cells to endothelial dysfunction, LDL-p and inflammation, long enough and the conditions for disease can be met.

BP - a metric of endothelial dysfunction - BP above 115/75 results in an almost linear degradation of endothelial function.

HDL cholesterol - this is a very indirect measure of oxidized LDL - HDL decreases the risk of LDL-p becoming oxidized and stuck in the subendothelial space. Higher levels of HDL are thus generally thought of as protective. Unfortunately, what we measure with HDL is the quantity of cholesterol that the HDL lipoprotein is carrying - not the functional capacity of HDL - which is what we really want to measure and understand.

Total Cholesterol - this is a metric that, on it’s own, is virtually meaningless. In the context for Framingham, total cholesterol serves as a very poor proxy for LDL-p. Really the model underlying the Framingham calculation, does track non-HDL cholesterol which (Total C - HDL-C) and this represents that cholesterol that is carried in the ApoB100 containing particles - HDL, IDL and VLDL. Generally speaking the cholesterol content of non-HDL-C particles is concordant with LDL particle count - which is what really correlates with risk.

In my practice - I start with Framingham, but also try and gather more data to support my understanding of the three ingredients:Endothelial dysfunction - the biggest factors to consider are

BP - is it optimal? 115/75

Does the patient smoke?

Are they obese?

Do they exercise?

What is their nutrition?

What is their TG/HDL ratio? This gives me an understanding of insulin resistance - which is associated with endothelial dysfunction as well as inflammation.

I can also measure asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) - these toxic non proteinogenic amino acids are potent inhibitors of nitric oxide as a result cause endothelial dysfunction.

Oxidized LDL:

What is their LDL-C?

What is their Apo-B100 - this essentially tells me their LDL-p, as each LDL has a single ApoB100 protein.

If there is a family history of premature heart disease, I will get an Lp(a) - more on this at another time…

If we look at atherosclerosis causality having three legs to the stool - then this is the leg that I have the most definitive information.

I can go further and measure oxLDL, a measure of circulating oxidized LDL cholesterol in circulation that correlates with LDL-C that has been oxidized in arteries.

I can also measure myeloperoxidase (MPO) - an enzyme released by immune cells as part of the oxidation and inflammation process at the root of atherosclerosis. MPO targets HDL - oxidizing the Apo-A1 protein and inhibiting HDL from protecting the LDL-p from oxidation.

Similarly, I can measure lipoprotein-associated phospholipase A2 (Lp-PLA2) - another inflammatory enzyme involved in the development of atherosclerosis.

(Some of these tests are only possible when the patient’s budget permits as not all of these tests are insured.)

Inflammation:

What is the patient’s high sensitivity C-reactive protein (hsCRP)? This is our best measure of chronic low grade inflammation. Unfortunately it does not tell us what is happening in the arteries.

Fibrinogen and ferritin are also key markers of systemic inflammation that can help us further understand risk.

Testing allows us to understand risk at a personal level, from here, my objective is to align my patient’s behavior with optimizing and reducing the risk across the three dimensions of atherosclerosis causality.The first place to start is with weight management - bringing the patient to normal levels of BMI, body fat and most importantly visceral fat will improve blood pressure, decrease insulin resistance, improve endothelial function, improve lipoproteins by increasing HDL-C and decreasing LDL-p, and decrease inflammation.For weight management - we nutrition comes first. Whole foods, mostly plant-based. We adjust and refine depending on response on our key biomarkers.Next we increase exercise. Our first goal is to get people to 150 minutes of moderate to vigorous exercise. Nothing magic here - there is ample evidence to support this level of exercise as the minimal effective dose. We adjust exercise across three components - aerobic, functional movement and resistance training. Again we adjust and refine depending on response of the patient’s biomarkers.Inadequate sleep and chronic stress have both been shown to affect inflammation, immune response and endothelial function - so we need to have a strategy to get at least 7 hours of high quality sleep and reduce stress.At Wellness Garage - we create month personalized lifestyle behavior action plans that we call “Precision Health Tune-ups”. We reassess every 4 months, until we have optimized behavior and reduced risk.If we see a patient’s measures of endothelial function, LDL and inflammation come to optimal levels with lifestyle measures we feel very comfortable that we have reduced their risk.When risk remains, we are comfortable with using both specific supplements and drug therapies to normalize BP, address LDL-p and other key biomarkers - there is, we believe, enough evidence to support this approach. In every case - this is a personal risk reduction conversation. Drug treatments are used to lower the probability of clinical atherosclerosis and carry a risk of adverse drug reactions. How much risk is too much on either side (disease vs drug reaction) of this decision is very individual - and can only be decided by a very well informed patient.

In summary, atherosclerosis is a systemic, almost ubiquitous disease process with three major causal dimensions.

Endothelial function

Oxidized LDL

Inflammation

Understanding your risk of atherosclerosis depends on understanding these dimensions.The place to start is with a medical assessment that measures at a minimum the key biomarkers for each dimension. Know your numbers.

With this baseline, you will have an understanding of how your genes and current behaviors are working for you.

The next step is to optimize your behaviors - nutrition, exercise, sleep, stress tolerance all play a role. After several months of modified behaviors, checking to see your body’s response allows you to optimize your behaviors and reduce risk.

If, despite optimal behavior change, your risk does not seem to come down - supplements and medications may help. This is something that you need to work through with your physician.​At Wellness Garage - we take a precision health approach to atherosclerosis prevention, treatment and reversal, by working with our members throughout this process - Assess, Change Behaviors, Re-assess and Adjust. If you would like our help to take control of your health please books free consultation.